{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,19]],"date-time":"2026-09-19T10:16:26Z","timestamp":1789812986602,"version":"4.0.1"},"reference-count":64,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2017,4,1]],"date-time":"2017-04-01T00:00:00Z","timestamp":1491004800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2017,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Both microbial infection and sterile inflammation augment bone marrow (BM) neutrophil production, but whether the induced accelerated granulopoiesis is mediated by a common pathway and the nature of such a pathway are poorly defined. We recently established that BM myeloid cell\u2013derived reactive oxygen species (ROS) externally regulate myeloid progenitor proliferation and differentiation in bacteria-elicited emergency granulopoiesis. In this article, we show that BM ROS levels are also elevated during sterile inflammation. Similar to in microbial infection, ROS were mainly generated by the phagocytic NADPH oxidase in Gr1+ myeloid cells. The myeloid cells and their ROS were uniformly distributed in the BM when visualized by multiphoton intravital microscopy, and ROS production was both required and sufficient for sterile inflammation\u2013elicited reactive granulopoiesis. Elevated granulopoiesis was mediated by ROS-induced phosphatase and tensin homolog oxidation and deactivation, leading to upregulated PtdIns(3,4,5)P3 signaling and increased progenitor cell proliferation. Collectively, these results demonstrate that, although infection-induced emergency granulopoiesis and sterile inflammation\u2013elicited reactive granulopoiesis are triggered by different stimuli and are mediated by distinct upstream signals, the pathways converge to NADPH oxidase\u2013dependent ROS production by BM myeloid cells. Thus, BM Gr1+ myeloid cells represent a key hematopoietic niche that supports accelerated granulopoiesis in infective and sterile inflammation. This niche may be an excellent target in various immune-mediated pathologies or immune reconstitution after BM transplantation.<\/jats:p>","DOI":"10.4049\/jimmunol.1602006","type":"journal-article","created":{"date-parts":[[2017,2,25]],"date-time":"2017-02-25T01:40:34Z","timestamp":1487986834000},"page":"2854-2864","source":"Crossref","is-referenced-by-count":35,"title":["Reactive Oxygen Species\u2013Producing Myeloid Cells Act as a Bone Marrow Niche for Sterile Inflammation\u2013Induced Reactive Granulopoiesis"],"prefix":"10.1093","volume":"198","author":[{"given":"Haiyan","family":"Zhu","sequence":"first","affiliation":[{"name":"The State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College , Tianjin 300020,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7070-6066","authenticated-orcid":false,"given":"Hyun-Jeong","family":"Kwak","sequence":"additional","affiliation":[{"name":"Department of Pathology, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peng","family":"Liu","sequence":"additional","affiliation":[{"name":"The State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College , Tianjin 300020,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Besnik","family":"Bajrami","sequence":"additional","affiliation":[{"name":"Department of Pathology, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0576-3907","authenticated-orcid":false,"given":"Yuanfu","family":"Xu","sequence":"additional","affiliation":[{"name":"The State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College , Tianjin 300020,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6385-4132","authenticated-orcid":false,"given":"Shin-Young","family":"Park","sequence":"additional","affiliation":[{"name":"Department of Pathology, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cesar","family":"Nombela-Arrieta","sequence":"additional","affiliation":[{"name":"Department of Pathology, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4852-0369","authenticated-orcid":false,"given":"Subhanjan","family":"Mondal","sequence":"additional","affiliation":[{"name":"Department of Pathology, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroto","family":"Kambara","sequence":"additional","affiliation":[{"name":"Department of Pathology, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongbo","family":"Yu","sequence":"additional","affiliation":[{"name":"Department of Hematopathology, VA Boston Healthcare System , West Roxbury, MA 02132"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li","family":"Chai","sequence":"additional","affiliation":[{"name":"Department of Pathology, Brigham and Women\u2019s Hospital, Harvard Medical School , Boston, MA 02115"},{"name":"Joint Program in Transfusion Medicine, Brigham and Women\u2019s Hospital, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leslie E","family":"Silberstein","sequence":"additional","affiliation":[{"name":"Department of Pathology, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4395-1095","authenticated-orcid":false,"given":"Tao","family":"Cheng","sequence":"additional","affiliation":[{"name":"The State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College , Tianjin 300020,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongbo R","family":"Luo","sequence":"additional","affiliation":[{"name":"Department of Pathology, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2017,4,1]]},"reference":[{"key":"2025030615061524000_r1","doi-asserted-by":"crossref","first-page":"1663","DOI":"10.1016\/j.cell.2015.11.013","article-title":"Transcriptional heterogeneity and lineage commitment in myeloid progenitors. 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